Evidence map›Paper›PMID 26472811›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015

Cigarette smoke has sensory effects through nicotinic and TRPA1 but not TRPV1 receptors on the isolated mouse trachea and larynx.

Tatjana I Kichko, Gerd Kobal, Peter W Reeh

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. The Role of TRP Channels in Nicotinic Provoked Pain and Irritation from the Oral Cavity and Throat: Translating Animal Data to Humans.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2022
    Review
  10. Sensory Effects of Nicotine and Tobacco.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021
    Review
  16. Sensory Innervation of the Larynx and the Search for Mucosal Mechanoreceptors.Journal of speech, language, and hearing research : JSLHR · 2021
    Article
  17. Effect ofJournal of personalized medicine · 2021
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Tatjana I KichkoInstitute of Physiology and Pathophysiology, Friedrich-Alexander-University of Erlangen-Nürnberg, Erlangen, Germany; and.
Gerd KobalAltria Client Services Inc., Richmond, Virginia.
Peter W ReehInstitute of Physiology and Pathophysiology, Friedrich-Alexander-University of Erlangen-Nürnberg, Erlangen, Germany; and peter.reeh@fau.de.ORCID 0000-0002-4367-094X
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEAltria (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoke (CS) exposes chemosensory nerves in the airways to a multitude of chemicals, some acting through the irritant receptors TRPV1 and TRPA1 but potentially also through nicotinic acetylcholine receptors (nAChR). Our aim was to characterize the differences in sensory neuronal effects of CS, gas phase, and particulate matter as well as of typical constituents, such as nicotine and reactive carbonyls. Isolated mouse trachea and larynx were employed to measure release of calcitonin gene-related peptide (CGRP) as an index of sensory neuron activation evoked by CS, by filtered CS gas phase essentially free of nicotine, and by dilute total particulate matter (TPM) containing defined nicotine concentrations. With CS stimulation of the superfused trachea, TRPV1 null mutants showed about the same large responses as wild-type mice, whereas both TRPA1(-/-) and double knockouts exhibited 80% reduction; the retained 20% response was abolished by mecamylamine (10 μM), indicating a distinct contribution of nAChRs. These phenotypes were accentuated by using TPM to stimulate the immersed trachea; 50% of response was retained in TRPA1(-/-) and abolished by mecamylamine. In contrast, the gas phase acted like a sheer TRPA1 agonist, consistent with its composition, among other compounds, of volatile reactive carbonyls like formaldehyde and acrolein. In the trachea, the gas phase and CS were equally effective in releasing CGRP, whereas the larynx showed much larger CS than gas phase responses. Thus nicotinic receptors contribute to the sensory effects of cigarette smoke on the trachea, which are dominated by TRPA1. How this translates to human perception affords future research.

Indexed as

AnimalsCalcitonin Gene-Related PeptideFemaleHumansIn Vitro TechniquesLarynxMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, NicotinicSensory Receptor CellsSmokeSmokingTracheaTransient Receptor Potential ChannelsCalcitonin Gene-Related PeptideReceptors, NicotinicSmokeTransient Receptor Potential ChannelsTRPA1 Cation ChannelTrpa1 protein, mouseTRPV1 protein, mouseTRPV Cation Channelscamphorgas phasemecamylamineparticulate matter

Identifiers

PMID26472811
PMCPMC4609941
OpenAlexW2289331117

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.